New research in mice questions the idea that "you can't teach an old dog new tricks." The answer may lie in preserving the blood-encephalon barrier, which tends to get leaky with age.

seniors doing a crossword together Share on Pinterest
New research looks at the decline of brain functions that accompanies aging.

The blood-brain barrier is a complex prepare of blood vessel characteristics that help shield the encephalon from potentially harmful substances in the bloodstream.

In a recent Science Translational Medicine study, scientists describe how the breakup of the claret-brain barrier can trigger encephalon inflammation and cognitive impairment in aging mice.

The international team constitute that the breakup of the blood-brain barrier activates a signaling protein in brain cells chosen astrocytes.

The researchers so developed and tested a drug that blocked the signaling protein, which goes by the name transforming growth factor-beta (TGF-beta).

After treatment with the drug, the mice showed fewer signs of encephalon inflammation and an improved power to learn new tasks that matched the performance of much younger mice.

"Nosotros tend to call back about the aged brain in the same mode nosotros remember near neurodegeneration: Historic period involves loss of function and dead cells," says co-senior report writer Daniela Kaufer, a professor of integrative biology at the Academy of California, Berkeley.

"But our new data tell a dissimilar story about why the aged brain is not performance well: Information technology is because of this 'fog' of inflammatory load," she adds.

Prof. Kaufer explains that within days of abolishing the "inflammatory fog," the aged encephalon starts to office more than similar a immature brain.

The findings should help scientists ameliorate understand the decline of brain functions involving inflammation that can accompany aging and atmospheric condition such as dementia.

An increasing body of enquiry — including imaging studies past co-senior study writer Alon Friedman, of Ben-Gurion University of the Negev in Israel and Dalhousie University in Canada — shows that the claret-brain barrier becomes less efficient with age.

The leakier the blood-encephalon barrier becomes, the easier information technology is for substances that cause inflammation to cantankerous over from the bloodstream into brain tissue and damage cells.

Kaufer and Friedman are also co-senior authors of another recent Science Translational Medicine study that took a closer look at inflammatory fog in leaky blood-brain barriers.

People with Alzheimer's affliction may oft experience epileptic events, but they and their doctors are not necessarily enlightened of them.

Advancing age is a run a risk factor for both Alzheimer's and epilepsy, and experimental and clinical data support the thought of a link between the two conditions.

For the second study, the squad analyzed EEG readings from people with Alzheimer's disease and establish an EEG signature for what they draw as "paroxysmal slow wave events (PSWEs)."

From the EEGs, they saw how the rate of PSWEs seemed to lucifer the level of cognitive impairment of the individuals.

In EEGs of people with epilepsy, they found that PSWEs that occurred between seizures matched areas of leaky blood-brain barrier. They plant the aforementioned lucifer in aged mice, mice prone to Alzheimer'southward illness, and rats with induced epilepsy.

Additional tests in young rats revealed that information technology was possible to impair the blood-brain barrier past introducing the protein albumin into the brain. This led to a higher rate of PSWEs.

In earlier research, Friedman and Kaufer had shown that albumin can leak into the brain post-obit trauma. The protein attaches itself to the TGF-beta receptor of astrocytes.

By binding to astrocytes' TGF-beta receptors, the protein sets off a concatenation of inflammation events that damage brain cells and circuits.

The damage increases the likelihood of seizures by disrupting the balance between excitation and inhibition of neurons.

The squad concludes that the findings point to a leaky blood-brain barrier as a potential crusade of nonconvulsive seizures in people with Alzheimer's disease. It may besides offering a potential treatment target.

The researchers suggest that the two sets of findings offer ii new biomarkers that could assistance doctors identify individuals who might have a blood-encephalon barrier problem: 1 using MRI (which tin can detect leaky barriers), and the other using EEG (which can detect aberrant brain rhythms).

There is also scope to develop the drug that they used every bit a way to repair a leaky blood-encephalon barrier to dull and possibly fifty-fifty reverse some of the problems that it tin can cause.

"We now have two biomarkers that tell you exactly where the blood-brain barrier is leaking, so yous can select patients for treatment and make decisions about how long you give the drug."

Prof. Daniela Kaufer

Experts commenting on the two studies generally welcome the findings but warn confronting jumping to the conclusion that they describe ways to contrary dementia in humans.

"Overall," notes Diego Gomez-Nicola, an associate professor of neuroscience at the University of Southampton in the United Kingdom, "these studies add together to a trunk of knowledge supporting the affect of inflammation on dementia, and provide promising targets for future clinical studies."